***本文章已被撤回***

Purpose: The long non-coding RNA cancer susceptibility 19 (CASC19 ) is recognized as an important regulator in gastric cancer, colorectal cancer, and non-small cell lung cancer. Nevertheless, to the best of our knowledge, the expression status and detailed roles of CASC19  in clear cell renal cell carcinoma (ccRCC) have not been elucidated. Hence, we aimed to determine CASC19  expression in ccRCC and investigate its roles in ccRCC oncogenicity. The molecular mechanisms underlying CASC19  functions in ccRCC were also determined.
Methods: CASC19  expression was measured by using reverse transcription-quantitative polymerase chain reaction. The effects of CASC19  on ccRCC cell proliferation, colony formation, migration, and invasiveness in vitro, as well as on tumor growth in vivo, were examined by the MTT assay, colony formation assay, cell migration and invasiveness assays, and tumor xenograft in nude nice, respectively.
Results: CASC19  was overexpressed in ccRCC tissues and cell lines. High expression of CASC19  was closely associated with unfavorable clinicopathological parameters and predicted negative clinical outcomes in patients with ccRCC. Knockdown of CASC19  decreased ccRCC cell proliferation, colony formation, migration, and invasiveness, as well as attenuated tumor growth in vivo. Mechanistically, CASC19  functioned as a competing endogenous RNA and upregulated the expression of ETS proto-oncogene 1 (ETS1) through sponging microRNA-532 (miR-532). Furthermore, rescue assays revealed that inhibiting miR-532 or restoring ETS1 expression partially abolished the impacts of CASC19  knockdown on ccRCC cells.
Conclusion: The CASC19/miR-532/ETS1 regulatory pathway is crucial for the malignant manifestations of ccRCC, which makes it an attractive target for potential treatments of ccRCC.
Keywords: cancer, MTT assay, cell migration, invasiveness, xenograft, knockdown